Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

50 prostate carcinomas which were totally prostatectomized together with removal of the seminal vesicles in all cases and pelvic lymphadenectomy in 38 cases were studied histologically. The material was cut by step-section technique in 5 mm thick slices and "large area slides" were made. 4 of the 50 carcinomas were morphologically circumscribed (stage I), 6 tumors were limited to the organ (stage II) and 40 prostate carcinomas had already penetrated the capsule, i.e. fascia of Denonvillier (stage III). In 12 cases the seminal vesicles were involved, regional lymph node metastases were seen 8 times. The carcinomas were mainly localized in the peripheral part of the organ (28 X in the periphery, 21 X both peripherally and centrally and only 1 X in the centre). Multifocal tumor growth was found in 30 cases (60%). The main mass of tumor was mostly situated in the middle (25 X) and caudal (15 X) zone of the prostate. During the course of tumor growth the expansion was directed centrally but then mainly longitudinal and parallel to the urethra. By progressing tumor volume there was a noticeable increase in capsular penetration as well as infiltration of the seminal vesicles and lymph node metastases. Histologically 10 carcinomas showed a uniform pattern, a unique solid and/or cribriform tumor architecture was never observed. 90% of the pluriform carcinomas consisted of the morphological stage III.
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PMID:Carcinoma and dysplastic lesions of the prostate. A histomorphological analysis of 50 total prostatectomies by step-section technique. 13 94

The potential modifying effects of testosterone propionate (TP) and high-caloric high-fat diet (20% corn oil, HF) on rat accessory sex gland carcinogenesis were investigated. Male F344 rats were treated five times at 4-week intervals with N-methylnitrosourea (MNU) i.v. or N-nitrosobis(2-oxopropyl)amine (BOP) s.c., each injection following 2 weeks pretreatment with dietary ethinyl estradiol. After completion of this carcinogen administration stage, animal groups received subcutaneous implantation of Silastic tubes filled with 40 mg TP with or without HF for 40 weeks. Carcinomas of the seminal vesicles and/or coagulating glands were induced in 5, 39 and 56% of rats given MNU alone, MNU and TP, and MNU and HF plus TP respectively. No equivalent tumors were found in rats given MNU and HF. In the BOP-treated groups, 11% of animals receiving TP but no HF diet demonstrated seminal vesicle carcinomas and 6% of rats receiving TP plus HF diet had coagulating gland carcinoma. Thus while TP exerted a strong enhancing effect on tumor growth in the seminal vesicles and coagulating glands, high caloric HF did not manifest any significant influence.
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PMID:Induction of invasive carcinomas of the seminal vesicles and coagulating glands of F344 rats by administration of N-methylnitrosourea or N-nitrosobis(2-oxopropyl)amine and followed by testosterone propionate with or without high-fat diet. 193 6

Inhibitory effects of the sustained delivery systems (microcapsules and microgranules) of a potent antagonist of luteinizing hormone-releasing hormone N-Ac-[3-(2-naphthyl)-D-alanine1, 4-chloro-D-phenylalanine2, 3-(3-pyridyl)-D-alanine3, D-citrulline6, D-alanine10]LH-RH (SB-75) on the growth of experimental prostate cancers were investigated. In the first experiment, three doses of a microcapsule preparation releasing 23.8, 47.6, and 71.4 micrograms of antagonist SB-75 per day were compared with microcapsules of agonist [D-Trp6]LH-RH liberating 25 micrograms/day in rats bearing Dunning R3327H transplantable prostate carcinoma. During 8 weeks of treatment, tumor growth was decreased by [D-Trp6]LH-RH and all three doses of SB-75 as compared to untreated controls. The highest dose of SB-75 (71.4 micrograms/day) caused a greater inhibition of prostate cancer growth than [D-Trp6]LH-RH as based on measurement of tumor volume and percentage change in tumor volume. Doses of 23.8 and 47.6 micrograms of SB-75 per day induced a partial and submaximal decrease, respectively, in tumor weight and volume. Tumor doubling time was the longest (50 days) with the high dose of SB-75 vs. 15 days for controls. The body weights were unchanged. The weights of testes, seminal vesicles, and ventral prostate were greatly reduced in all three groups that received SB-75, and testosterone levels were decreased to nondetectable values in the case of the two higher doses of SB-75. LH levels were also diminished. Similar results were obtained in the second experiment, in which the animals were treated for a period of 8 weeks with microgranules of SB-75. Therapy with microgranules of SB-75 significantly decreased tumor growth as measured by the final tumor volume, the percentage change from the initial tumor volume, and the reduction in tumor weight. The results indicate that antagonist SB-75, released from sustained delivery systems, can produce a state of chemical castration and effectively inhibit the growth of experimental prostate cancers. The efficacy of the antagonist SB-75 in inhibiting androgen-dependent Dunning prostatic carcinoma and the absence of side effects suggest its possible usefulness for the treatment of hormone-sensitive tumors.
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PMID:Inhibition of growth of experimental prostate cancer with sustained delivery systems (microcapsules and microgranules) of the luteinizing hormone-releasing hormone antagonist SB-75. 199 76

Rats bearing Dunning R-3327 hormone-dependent prostate tumors were treated with LH-RH antagonist SB-75 in the form of microcapsules for sustained delivery administered every 3 weeks and which released 24, 48, 72 micrograms/day respectively. The effects were compared with those of microcapsules of the agonist D-Trp-6-LH-RH releasing 25 micrograms/day. Both types of LH-RH analogs significantly inhibited tumor growth over a period of treatment lasting 8 weeks. The effect of SB-75 was dose-dependent. The total inhibition of spermatogenesis, as well as atrophic signs in the prostate and seminal vesicles, demonstrated a marked suppression of the pituitary-gonadal system by these analogs. The histological signs of tumor regression were analyzed. The vascular content of tumors did not change after the treatments, but an increased amount of connective tissue was found in the treated tumors, especially after administration of SB-75. Both the agonist and the antagonist caused a moderate decrease of the number of mitotic cells and a marked increase of apoptosis in the tumors. The apoptotic index, i.e. the percentage of tumorous glands showing signs of apoptosis, reached 40-50% in treated groups, compared to only 15% in controls. An apoptotic index of 60% was noted in a separate group of rats treated with 200 micrograms SB-75/animal/day for 3 days. The signs of enhanced apoptosis disappeared 1 week after the short-term treatment. The induction of apoptosis by LH-RH analogs seemed to be of greater importance in tumor growth inhibition than their antimitotic effect. These results extend our previous observations on the efficacy of LH-RH antagonists in inhibition of various cancers. This histopathologic evaluation clearly supports our contention that modern antagonists of LH-RH, free of edematogenic effects, inhibit the growth of Dunning prostate tumors. Because of the immediate inhibitory effects, the use of LH-RH antagonists might lead to an improvement in the clinical response in patients with prostate cancer.
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PMID:Histological changes in Dunning prostate tumors and testes of rats treated with LH-RH antagonist SB-75. 202 Jun 21

We had previously reported that 6-methylene progesterone, an inhibitor of 5 alpha-reductase, the enzyme which converts testosterone to dihydrotestosterone, markedly inhibited growth of the androgen-dependent Dunning R3327-H rat prostatic tumors. We now find that the progesterone derivatives melengestrol acetate (MGA) and megestrol acetate (MA) inhibit both the androgen-dependent (Dunning R3327-H) and the androgen-independent (Dunning R3327-AT3) prostatic tumors. Growth of the AT3 tumors was suppressed by approximately 53% after 9 days of daily s.c. injections with MGA at 10 mg/kg body weight. MGA also caused a 54% weight reduction of the ventral prostate and a 53% reduction of the seminal vesicles. Adrenal weights were reduced by 42%. A 24-day oral treatment with MGA (at approximately 15-17 mg/(kg.day)) inhibited AT3 tumor growth by 59% and caused a weight reduction in the following tissues: prostate (46%), seminal vesicles (19%), testes (12%), and adrenals (52%). Under the same protocol, MA inhibited AT3 tumor growth by 32% and reduced the weight of the ventral prostate by 49% and the weight of the adrenals by 18%, but had no effect on the seminal vesicles and testes. The extent of the MGA-induced prostatic regression was accompanied by cytological changes similar to those effected by 6-methylene progesterone, i.e., shrinking of the acinar epithelium. The AT3 tumors in MGA-treated rats displayed a limited degree of apoptosis. Atrophy of the adrenal cortex and lowered plasma levels of corticosterone and dihydroepiandrosterone were also observed. A therapeutic role for MGA and MA against androgen-independent prostatic neoplasms in man is forecast by these observations.
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PMID:Melengestrol acetate and megestrol acetate are prostatic tumor inhibiting agents. 226 13

The antitumoral activity of a novel imidazole derivative, R 75,251, has been studied in the androgen-dependent R3327G Dunning prostate adenocarcinoma grafted subcutaneously in syngeneic rats. Dietary application resulting approximately in dose levels of 80, 120, and 160 mg/kg reduced tumor weight by 66, 81, and 79%, respectively. This effect was not significantly different from that measured after castration (-82%). In intact animals, however, serum testosterone levels were almost not affected by R 75,251 treatment while LH levels rose two- to threefold. In castrated rats a tenfold increase in LH was observed. Moreover, prostate and seminal vesicles weights decreased much less after R 75,251 treatment than after castration. In castrated animals, treatment with R 75,251 induced a slight, non-significant reduction in tumor weight (-36%) compared with castration alone. In castrated animals, tumor growth was restored by exogenous administration of testosterone. In such animals R 75,251 also significantly reduced tumor weight by 57%. Similar results were obtained with Dunning R3327G prostate adenocarcinoma grafted beneath the renal capsule in male syngeneic rats receiving twice daily orally by gavage a dose of 80 mg/kg of R 75,251. These data suggest that R 75,251 exerts an antitumoral effect independent of its inhibition of androgen biosynthesis.
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PMID:Antitumoral effects of R 75251 on the growth of transplantable R3327 prostatic adenocarcinoma in rats. 237 Nov 76

Cells from the PC-3 human prostate cancer cell line were evaluated in athymic nude mice in order to determine the influence of size of the primary tumor and site inoculation on the incidence and pattern of metastasis. At autopsy, all organs, including the skeleton, were evaluated for metastasis. Subcutaneous injections resulted in metastases to the draining axillary lymph node and lungs (56% and 13%, respectively), and were correlated with size of the primary tumor. Tail vein injection resulted in a high incidence of lung metastasis, while injection into the peritoneal space, spleen, and seminal vesicles resulted in intraabdominal tumor growth, liver metastasis, and large tumors within the seminal vesicles, respectively. Skeletal metastases were not observed in any of the animals studied. We conclude that injection of PC-3 cells into various sites results in different patterns of metastasis, but may not constitute an entirely suitable animal model of human prostate cancer due to the lack of metastasis to the skeleton.
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PMID:Patterns of metastasis by the human prostate cancer cell line PC-3 in athymic nude mice. 252 82

The fate of 48 patients with clinical stage T3 prostatic carcinoma after attempted curative surgical management was studied. In 23 of these patients positive frozen sections of the lymph nodes were found at pelvic lymphadenectomy and orchiectomy was performed. The median interval to progression was 61 months. Radical prostatectomy was performed in the remaining 25 patients. In 4 of these patients positive lymph nodes were found on paraffin sections but no additional treatment was given. Over-all, total tumor removal as defined by negative lymph nodes and negative margins of resection could be achieved in 14 of the 48 patients (29 per cent). During the same period 34 patients with clinical state T less than 3 prostatic carcinoma were treated in a similar manner. Orchiectomy was done in 4 patients because of positive frozen sections of the lymph nodes and radical prostatectomy was done in 30, including 1 in whom positive paraffin sections of the lymph nodes were found but no additional treatment was given. An attempt was made to study the impact of several prognostic factors by comparing the probability of progression between patients with stage pT3 disease with (T3pT3N0) or without (T less than 3pT3N0) extracapsular tumor growth as determined by preoperative rectal examination (36 versus 27 per cent progression at 3 years), with or without positive margins of resection (45 versus 20 per cent progression at 3 years) and with or without involvement of the seminal vesicles (47 versus 18 per cent progression at 3 years). Our results suggest that a certain proportion of patients with clinical stage T3 disease will benefit from radical prostatectomy. This is to be expected especially in patients with stage T3pT3N0 cancer and negative margins.
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PMID:Surgical treatment of locally advanced (T3) prostatic carcinoma: early results. 365 37

Experiments were performed to observe the role of estrogen receptor in the proliferation of androgen-dependent mouse tumor, Shionogi carcinoma 115. Estradiol and diethylstilbestrol inhibited tumor growth as well as the weight gain of seminal vesicles and prostate glands in intact male mice. Tamoxifen decreased the tumor weight in intact males. Both nitromifene given to intact mice and tamoxifen given to castrated androgenized mice decreased the weight of seminal vesicles, but increased tumor weight. Estradiol was bound to the androgen receptor of the tumor cytosol with relatively high affinity, whereas diethylstilbestrol, tamoxifen and nitromifene were not. These were effective competitors in the estrogen receptor present in the tumor cytosol. These results suggest that the estrogen receptor system in Shionogi carcinoma 115 inhibits the proliferation of tumor cells.
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PMID:Effects of estrogens and antiestrogens on androgen-dependent growth of Shionogi carcinoma 115: role of estrogen receptor. 674 83

Studies were undertaken to examine the effects of an estradiol-chemical delivery system (E2-CDS) or castration (CAST) on plasma testosterone (T) and growth of the Segaloff 11095 carcinoma. Fischer 344 rats were implanted subcutaneously with the Segaloff 11095 tumor and tumor growth was monitored thereafter. After optimal tumor growth, when the average tumor size was approximately 25 x 15 mm (length x width; 4-5 g wet weight), rats were randomized into (1) testis-intact controls; (2) CAST; (3) intact+E2-CDS groups (rats received weekly injection of the E2-CDS at 0.5 mg/kg). Animals were killed 7 or 14 days after the initiation of treatments. Blood and tissue samples were collected for subsequent analysis. Plasma T levels were suppressed by 98% and 97% through 14 days after CAST or E2-CDS treatment. CAST increased plasma gonadotropin (LH) concentrations, while E2-CDS reduced LH compared to intact control levels. E2-CDS treatment increased plasma E2 levels to 24 (one injection) or 75 pg/ml (two injections) at 7 or 14 days, respectively. E2-CDS, given once a week for 2 consecutive weeks, resulted in a decreased growth of the prostate tumor by 61%, while CAST reduced the weights of these tumors by only 20%. In response to E2-CDS (one or two injections), weights of the in situ ventral prostate and seminal vesicles were significantly reduced by 70% and 50%, respectively, in tumor-bearing rats. Similarly, CAST reduced the weights of these tissues by 80% (prostate) or 52% (seminal vesicle) at 7 or 14 days after treatment. Pituitary weight increased, while testes weight decreased by 20% with two injections of E2-CDS, compared with intact control rats. Collectively, these data indicate that E2-CDS is effective in reducing the growth rate of prostatic tumors in the rat.
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PMID:Suppression of plasma testosterone and prostate carcinoma size by a redox-based, brain-targeted estrogen delivery system in the rat. 833 87


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